Aim Leptin is an important peptide hormone that regulates food intake and plays a crucial role in modulating olfactory function. Although a few previous studies have investigated the effect of leptin on odor perception and discrimination in rodents, research on the neural basis underlying the behavioral changes is lacking. Here we study how leptin affects behavioral performance during a go/no‐go task and how it modulates neural activity of mitral/tufted cells in the olfactory bulb, which plays an important role in odor information processing and representation. Methods A go/no‐go odor discrimination task was used in the behavioral test. For in vivo studies, single unit recordings, local field potential recordings and fiber photometry recordings were used. For in vitro studies, we performed patch clamp recordings in the slice of the olfactory bulb. Results Behaviorally, leptin affects performance and reaction time in a difficult odor‐discrimination task. Leptin decreases the spontaneous firing of single mitral/tufted cells, decreases the odor‐evoked beta and high gamma local field potential response, and has bidirectional effects on the odor‐evoked responses of single mitral/tufted cells. Leptin also inhibits the population calcium activity in genetically identified mitral/tufted cells and granule cells. Furthermore, in vitro slice recordings reveal that leptin inhibits mitral cell activity through direct modulation of the voltage‐sensitive potassium channel. Conclusions The behavioral reduction in odor discrimination observed after leptin administration is likely due to decreased neural activity in mitral/tufted cells, caused by modulation of potassium channels in these cells.

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To assess the actions of thiopental at the spinal dorsal horn level, we examined the effects of thiopental using the whole cell patch-clamp technique on mechanically dissociated rat spinal dorsal horn neurons. Thiopental, at large concentrations, elicited a current (I(Thio)) through activation of chloride conductance, and its threshold concentration was approximately 50 microM. I(Thio) was sensitive to bicuculline, a gamma-aminobutyric acid (GABA)A receptor antagonist, but not to strychnine, a glycine receptor antagonist. At a clinically relevant concentration (30 muM), thiopental markedly enhanced the peak amplitude of a subsaturating GABA-induced current (I(GABA)) but not that of a saturating GABA-induced current. Furthermore, thiopental prolonged the time constants of both desensitization and deactivation of I(GABA). At a large concentration (300 muM), it inhibited the peak amplitude of I(GABA), which may be the result of open-channel blockade. In addition, at 30 microM, thiopental increased the duration and decreased the frequency of GABAergic miniature inhibitory postsynaptic currents. These results indicate that thiopental enhances GABAergic inhibitory transmission and suggest that GABA(A) receptors in the spinal cord are a potential target through which thiopental causes immobility and depresses the response to noxious stimuli.

Aim:To investigate the possible role of hypothalamic kisspeptin in the regulation of body fluid metabolism and maintenance of internal homeostasis. Methods: Natriuresis and diuresis were induced by blood volume expansion (VE) in anesthetized male rats and kisspeptin-10 was intracerebroventricularly (icv) administered. Radioimmunoassay (RIA) was used to measure the plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations during the VE. The mediation of the renal sympathetic nerve was also investigated in rats with bilateral renal sympathetic denervation. Results: The increased urine flow and sodium excretion induced by VE were significantly inhibited by icv injection of 5 nmol kisspeptin-10 (P<0.05), which peaked 20 min after the decrease in VE. The mean arterial blood pressure and heart rate did not change during the experiment. Plasma AVP concentrations were significantly increased 20 min after icv injection of 5 nmol kisspeptin-10 during VE (P<0.05), while pretreatment with 5 nmol kisspeptin-10 did not significantly change plasma ANP concentrations. Furthermore, pretreatment with 5 nmol kisspeptin-10 could significantly inhibit VE-induced natriuresis and diuresis in renal sympathetic denervated rats (P<0.05). Conclusion: Central administration of kisspeptin-10 inhibited VE-induced natriuresis and diuresis. This effect was likely mediated by increasing AVP release independent of plasma ANP concentration and renal sympathetic nerve activity.

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Fiber photometry is a recently-developed method that indirectly measures neural activity by monitoring Ca2+ signals in genetically-identified neuronal populations. Although fiber photometry is widely used in neuroscience research, the relationship between the recorded Ca2+ signals and direct electrophysiological measurements of neural activity remains elusive. Here, we simultaneously recorded odor-evoked Ca2+ and electrophysiological signals [single-unit spikes and local field potentials (LFPs)] from mitral/tufted cells in the olfactory bulb of awake, head-fixed mice. Odors evoked responses in all types of signal but the response characteristics (e.g., type of response and time course) differed. The Ca2+ signal was correlated most closely with power in the β-band of the LFP. The Ca2+ signal performed slightly better at odor classification than high-γ oscillations, worse than single-unit spikes, and similarly to β oscillations. These results provide new information to help researchers select an appropriate method for monitoring neural activity under specific conditions.

Aim of the Study. This study aimed to systematically evaluate the effectiveness and safety of treating negative emotions after percutaneous coronary intervention (PCI) based on the theory of “harmonization of qi and blood.” Background. Many patients undergoing PCI have been reported to suffer from psychological distress and negative emotions. Several lines of evidence have indicated that PCI patients with negative emotions are particularly vulnerable to myocardial reperfusion injury when they face psychological challenges. As proven by clinical trials and research, traditional Chinese medicine (TCM) has certain advantages in alleviating psychological symptoms in PCI patients. The level of evidence for TCM is not yet high. There is no existing systematic review to evaluate the effectiveness and safety of TCM in post-PCI patients. Methods. PubMed, EMBASE, Cochrane Library, Web of Science, CNKI, VIP, Wanfang Database, and CBM were searched to identify randomized controlled trials (RCTs) that treated negative emotions after PCI using qi and blood cotherapy. The search period was from database inception to March 1, 2022. After applying the inclusion and exclusion criteria to the RCTs, research quality evaluation and data extraction were conducted, and a meta-analysis of the articles was performed using Revman 5.3 and Stata 12.1. Results. A total of 14 RCTs involving 1314 patients were included. Meta-analysis results indicated that compared with the anti-anxiety and depression medications group, the qi-blood harmony group was more effective in clinical outcomes (RR = 1.19, 95% CI (1.13, 1.25), P < 0.00001 ), maintaining the stability of angina pectoris (SMD = 0.65, 95% CI (0.29, 1.01), P = 0.0004 ), increasing the degree of patients’ satisfaction (SMD = 0.95, 95% CI (0.25, 1.65), P = 0.008 ), reducing the frequency of attacks (SMD = 0.64, 95% CI (0.11, 1.18), P = 0.02 ), and the incidence of adverse reactions (RR = 0.54, 95% CI (0.43, 0.68), P < 0.00001 ). The HAMA and HAMD scores were significantly lower after treatment, and there was no significant difference between the two groups (HAMA: RR = 1.03, 95% CI (0.95, 1.12), P = 0.4 ). The efficacy of the two groups was comparable. In terms of reduction of the HAMD score, after sensitivity analysis, the literature by Liang was found to be significantly influencing the results, and after excluding the results of Liang, the qi-blood harmony group was superior to the Western medicine group for reducing the HAMD score (RR = 1.12, 95% CI (1.01, 1.24), P < 0.05 ), which was significantly different. The results of this review, combined with the grade evaluation, suggest that the HAMA posttreatment score reduction, the efficacy of TCM treatment, and the incidence of adverse reactions were supported by moderate evidence, and the HAMD posttreatment score reduction and the SAQ score were supported by low-quality evidence. Conclusion. Treating negative emotions after PCI based on the idea of “harmonization of qi and blood” can effectively improve the clinical efficacy, the stability of angina pectoris and the degree of patient satisfaction, and can reduce the frequency of angina attacks and the incidence of adverse events. There was no significant difference between the two groups for reductions in the HAMA and HAMD scores. However, more high-quality, large sample, multicentre RCTs are still needed for further verification. PROSPERO Registration Number: PROSPERO CRD42022313169.

Glioblastoma (GBM) is a malignant tumor prone to recurrence and resistant to conventional therapies. GBM cells show high autophagy activity, contributing to its rapid progression. Casein kinase 1 family, such as Casein kinase 1α (CK1α), has shown its effect on autophagy by binding to the hypoxia-inducible factor-1α (HIF-1α). This study investigates the expression of CK1α and HIF-1α in healthy and GBM tissues and its relations with autophagy-related genes and GBM cell viability. The expressions of CK1α, HIF-1α, and autophagy-related proteins in normal tissues, GBM tissues, and GBM cell lines (U87MG, U251, U118-MG, LN229, SHG44) were analyzed by qRT-PCR and Western blotting. In vitro, the U87MG cell line was transfected with pcDNA3.1-CK1α to enhance the expression of CK1α or both pcDNA3.1-CK1α and siRNA-HIF-1α. The expression of CK1α, HIF-1α, and autophagy-related proteins in GBM brain tissues and cell lines was higher than in normal brain tissues. In U87MG cells, enhanced CK1α expression upregulated the expression of HIF-1α and autophagy-related proteins and promoted cell proliferation. Inhibiting the expression of HIF-1α reduced the expression of autophagy-related proteins and decreased U87MG cell viability. Overexpressed CK1α positively regulates autophagy activity through the HIF-1α pathway. Inhibition of CK1α might be a potential therapeutic approach for glioblastoma therapy.